Night 7k to 12k Chennai City Center Call Girls 👉👉 7427069034⭐⭐ 100% Genuine E...
CARDIOEMBOLIC S-1.pptx
1. CARDIOEMBOLIC STROKE;
THE BURDEN AND IMPACT OF
RHEUMATIC VALVULAR HEART
DISEASE
DEPARTMENT OF MEDICINE
LAUTECH TEACHING HOSPITAL
DR SOPE TOPE ORUGUN
4. Introduction
Stroke is defined as sudden onset
of focal or global neurological
deficit lasting more than 24hours
with no other apparent cause
apart from a vascular one.
5. Epidemiology
Stroke is the leading cause of adult disability
The 2nd leading cause of death; 6.5million in 2013
Up to 1million persons worldwide have an episode per year
750,000 incident cases in the US yearly, likely more in developing
countries
30% stroke affected workers proceed to lose their jobs because
of disabilities.
6. Epidemiology
The risk of stroke doubles with each decade after 55yrs
Blacks & Hispanics are twice at risk as whites
Men stand 40% higher chance of stroke than women worldwide
Hypertension increases risk 4folds
Smoking doubles the risk
On the average, someone in the US has stroke every 40secs and,
someone dies from stroke every 4mins
7. Epidemiology
KW Wahab reported 1.14/1000 cases incident rate in
hospital admission at UITH, Ilorin in 2008
Also, a 30day case fatality may be upto 40%.
Corroborated in 2015 by MA komolafe et al
Men are almost twice as affected as women before age
65, thereafter women predominate in NIgeria
8. Statistics
Type of stroke Percentage
Atherothrombotic 44%
Ischemic
84%
Cardioembolic 21%
Small vessel disease 19%
Intrcerebral
haemorrhage
10% Haemorrhagic
16%
Subarachnoid 6%
100%
9. Cardioembolic stroke
Embolism is the primary mechanism of stroke due to
heart diseases.
Thrombi form in the cardiac chambers and detach, and
get dislodged downstream.
If the thrombus lyses quickly, Transient Ischemic Attack
may occur.
Longer staying thrombus causes stroke
Embolic stroke tends to be sudden in onset with
maximal neurologic deficit all at once
10. Cardioembolic stroke
Middle cerebral Artery(MCA) and Posterior Cerebral
artery(PCA) are more affected then anterior cerebral
artery
MCA infarcts are usually extensive,
Branches 3-4mm wide, if occluded lead to cortical and
white matter infarcts
Location and extent of infarct depends on collateral
circulation
11. Cardioembolic Stroke
Mechnism of Cardioembolic stroke can be subsclassified:
a. Mural Emboli
b. Valvular heart disease
c. Arrhythmia
d. Paradoxical emboli
e. Septic Emboli
12. Cardioembolic Stroke
Causes:
Non rheumatic nonvalvular atrial fibrillation is
commonest cause worldwide
Myocardial infarction(MI)
Prosthetic valves
Rheumatic valvular heart disease
Ischaemic Cardiomyopathy
13. Cardioembolic Stroke
Presumed mechanism in Atrial fibrillation are:
Thrombus formation in fibrillating atrium
Atrial appendage detachment embolization
Average risk of stroke is 5%
CHADSVasc Score
14. Cardioembolic stroke
RVHD causes stroke when there is either prominent
mitral stenosis or atrial fibrillation
MI especially if transmural and anteroapical
predisposes to thrombus formation
Prophylactic anticoagulation has shown benefit in
stroke prevention.
15. Cardioembolic stroke
Paradoxical emboli
Arterial presence of a venous thrombus
Due to any of these:
patent foramen ovale
ASD
Pulmonary AV malformations
17. The link between Cardioembolic stroke and RHD is
important in this presentation, though being relatively
not as common as other causes, it may contribute to
early onset incapacitation of patients and increase
both morbidity and mortality.
18. Rheumatic heart disease
(RHD)
Rheumatic heart disease is a chronic autoimmune
inflammation of the heart structures especially the valves ,
following group A streptococcal infection which leads to
fibrosis and stenosis of the valves +/- regurgitations.
It is a chronic sequelae of Acute rheumatic fever
19. RHD
Rheumatic fever(RF) is an inflammatory disease that occurs as a
delayed non suppurative sequelae of upper respiratory tract infection
with group A streptococci.
In its classic form, the disorder is acute, febrile and largely self
limiting.
Damage to heart valves may however be chronic, progressive and
cause cardiac disability or death years down the line.
20. RHD
One of the major causes of cardioembolic stroke is
Rheumatic heart disease (RHD)
20% of stroke is due to cardioembolic origin, valvular
pathology contribute importantly to this, predisposing
to clot formation
RHD accounts for a small percentage of this
21. Rheumatic Heart Disease
Rheumatic heart disease is a chronic complication of
Rheumatic fever.
In the acute phase, there is inflammation of all layers
of the heart; pancarditis.
However there is a residual chronic sequelae of
valvular and endocardial fibrosis and stenosis.
Regurgitation may be present
22. Epidemiology
30 million cases worldwide in 2015
2.4million are children
Highest incidence of Rheumatic fever is between age
5-25.
Commoner in developing countries & marginalized
communities of developed countries.
Varies from 15.2 cases/100000 in Fiji to 1 case/100000
in USA
Rheumatic fever was the commnest indication for
valvular replacement before advent of adequate
prophylactic method
23. Epidemiology
Estimated 11.5 million disability adjusted life years lost
305,000 deaths are due to RHD/ year
Africa, SEA, Pacific Islanders account for 84% of
prevalence.
Females are twice as affected as males
Females account for 2/3 of hospitalized cases in 12
countries including India, Yemen, Africa
24. Epidemiology
In 2010, economic loss due to RHD is
$2200 billion (discounted)
$5400 billion (undiscounted)
Although, Africa has 10% of world population, it has
up to 50% of world RHD cases.
26. Pathogenesis
A. ORGANISM FACTOR
The development of RF, and RHD, requires an antecedent history
of infection of Group A Beta hemolytic streptococci ( GABHS)
Noteworthy is the fact that Cutaneous streptococcal infection
causing post streptococcal GN which was initially not thought to
cause RVHD, actually do – In aborigines in native Australasia
27. Pathogenesis
GABHS
Group A streptococci are pure human pathogens
a) Natural streptococcal infection in animals is rare
b) Lab animals are not models for human streptococcal infection e.g
scarlet fever, erysipelas,
c) A much higher dose of inoculum is needed to cause animal
infections
All group A streptococcal infection have highest incidence in
children lower than 10yrs
28. RF
Streptococcal Toxins
a) Capsule
b) Cell wall
c) M proteins
d) Streptolysin O
e) Streptolysin S
f) DNAse A-D
g) Pyrogenic exotoxins
h) Nicotine Adenine Dinucleotidase
31. Pathogenesis
B. HOST FACTORS
About 3% of population is susceptible to RF
Concordance among mono zygote twin shows
inherited susceptibility
HLA 2 is associated with susceptibility
Associations with mannose binding lectine &
polymorphism of TGF Beta 1 & Ig genes
32. Pathogenesis
C. IMMUNE RESPONSE
The basis is an autoimmune reaction in susceptible
hosts
Damage result from cross reaction between epitopes
of bost and organism
M proteins & Streptococcal N Acetyl glucosamine are
immunologically similar to molecules in human
myosin, tropomysin, keratin, actin, laminin, vimentin &
N acetyl glucosamine.
33. Pathogenesis
Cross reacting antibodies attach at the cardiac valve
endothelium.
This allows entry of primed CD4+ lymphocytes.
This leads to T Cell Mediated inflammation
34. Pathophysiology
Rheumatic fever , non suppurative complication of pharyngitis
caused by GABHS
Rheumatic heart disease is a Chronic sequelae
It usually occurs after repeated bouts of acute illness
The risk of developing ARF after an acute episode of GABHS
infection is said to be 0.3 – 3%
However, 60% of those with ARF develop RHD
35. Pathophysiology
ARF is a multisystemic disease.
Affects the Skin, joints, CNS,
Usually Acute rheumatic fever starts 1-3wks after
pharyngitis.
It has an average period of 20-40years before
development of Chronic Cardiac complications.
A history of Rheumatic Fever is positive in 60% of pure
mitral stenosis
36. Pathophysiology
It is an interplay of several factors.
Cellular immunity {Thelper 1 cells}
Humoral mediated immunity
Molecular mimicry
Genetic predisposition - HLA DR (familial studies)
The inflammation generated persists beyond the acute infection and
lead to the picture seen in ARF
37. Pathophysiology
Direct toxic effect theory
The antigen/ antibody complex formed after infection
with GABHS are in excess of what is needed and are thus
deposited on tissues in the body causing a direct toxic
effect in the valves and Glomeruli especially.
38. Pathophysiology
TCell responsive to Streptococcal M protein invade the
valve through the valvular endothelium
Antistreptococcal Carbohydrate stimulates T cell to
release TNF & Interleukins
Thelper 17 associated cytokines are increased in RHD
39. Pathophysiology
Streptococcal antigens display molecular mimicry
recognized by the human immune system.
M protein of GABHS mimics Cardiac Myosin & Valvular
Endothelium
40. Pathophysiology
The mitral valve is most affected, then- aortic, tricuspid &
Pulmonary
Mitral valve(MV) regurgitation is usually accompanied
with 1 or more other valves
It is said that in almost all acquired cases of MV stenosis,
RHD is the cause
It is on the downward trend in developed countries
41. Pathophysiology
Cell wall components - peptidoglycan, lipotechoic
backbone interact with host immunity.
M proteins A-D
Inhibit phagocytosis by leucocytes
B& C region camouflage the bacteria against
opsonization
42. Pathophysiology
Streptolysin O
A thiol activated cytolysin inhibited by Antibodies &
Cholesterol.
Capsule
Binds epithelial CD 44 and acts as antiphagocytic.
46. Revised Jones criteria
Major Criteria
Migratory polyarthritis 70%
Carditis 50- 60%
Syndeham Chorea < 15%
Subcutaneous Nodules rare in adults
Erythema Marginatum
47. Revised Jones Criteria
Minor Criteria
Clinical
Fever >38.5
Polyarthralgia(not considered if polyarthritis is a major
criterion)
Laboratory
Elevated ESR or WBCC
ECG: prolonged PR interval
48. Revised Jones Criteria
Supporting evidence of past GABHS infection
A positive throat culture
Rapid antigen testfor group A
Recent scarlet fever
49. Diagnostic criteria
1 major and 2 minor with evidence of GABSH
2 major criteria
2 minor criteria + previous throat infection with
GABHS
Patients presenting for the 1st time with Pure mitral
valve stenosis or mixed mitral valve disease and or
aortic disease.
They donot require any other criteria for diagnosis of
RHD
51. Complications
Cardiac involvements are most serious in ARF
60% of patients develop carditis in ARF
Add to prevalence rate of RHD of 15million world
wide
RHD predisposes to further cardiac damage with
subsequent bouts of infection
There is need for Secondary prophylaxis
52. Complications
Cardioembolic Stroke
Infective Endocarditis
Acute Pulmonary Edema
Cardiac failure
Death 1.5% of all patients annually
Increased Perinatal mortality
Cole & Adeleye et al 1982 revealed most of these
complications especially in Pregnancy women are due to
poor socioeconomic & healthcare facilities
53. Investigations
No single Laboratory result can diagnose RHD without
positive history
ESR or CRP are elevated, at times markedly
They useful in monitoring disease but sensitivity is poor
Throat culture – it is criterion standard for diagnosis of GABHS
Note that rapid antigen detection are not sensitive, but
specific
54. Investigations
ASO – elevated ASO shows previous or ingoing infection,
higher post pharyngitis than after skin infection
Blood culture may help rule out infective endocarditis,
bacteremia and disseminated gonococcal infection
55. Imaging studies
Echocardiography:
a) Valvular stenosis commonly Mitral()
b) Thickening of the valves
c) Calcification of valves and subvalvular apparatus
d) Regurgitations
e) Involvement if aortic valve may accompany but rarely
presents alone
60. ECG
ECG
May show prolonged PR interval
AV block
Repeat in 2 weeks and 2 months if prolonged PR
interval
61. Gross findings
Acute phase;
a) Small verrucuous endocarditis
b) Small uniformly sized thrombi with no vlave destruction
Chronic state:
a) Commisural fusion
b) Valve thickening
c) Shortened, fused subvalvular chorda – ‘fish mouth deformity’
d) Affectation of Mitral and aortic valves mostly
62.
63. Gross findings
Post rheumatic valve disease is generally diagnosed at surgery
Aortic stenosis is usually caused by degenerative calcific disease
50% of which is due to bicuspid aortic valve
Nodular calcific stenosis with calcific deposit in sinus of vasalva
sparing the free edges
Post rheumatic stenosis involves the edges, commisures and leaflets
64. Gross findings
Post rheumatic Mitral insufficiency
Closely related to mitral prolapse but differentiated by
Has Chordal fusion, thickening and shortening
65. Immunochemistry
Presence of CD 4 and CD 8 in T cell subsets in Acute rheumatic
fever valves
Major histocompatibility complex 2 (MHC-2) antigens are
expressed in blood vessel endothelial cells and fibroblasts
67. Microscopy
Vegetations in ARF shows surface thrombi, lack of
underlying valve destruction and mild edema,
Chronic RVHD shows neovascularization, chronic
inflammation and calcification. Her calcium is deposited in
the leaflet itself as opposed to annular calcification
68. Microscopy
Aschoff nodules are considered pathognomonic of
post rheumatic heart disease.
Interstitial fibroinflammatory lesions with
macrophages, and collagen necrosis
71. Management
1° prevention involves removal of of all factors that predispose to
streptococcal infection
Personal hygiene
Environmental Sanitation
Prevention of overcrowding
Governmental policies that favour reduction in the incidence of
RVHD
These are very difficult in developing countries where RF is common.
72. Management
Mainstay is thus Prophylaxis
Timely and complete treatment of streptococcal
infection
Requires:
a) Prompt presentation of patients to health facility
b) Availability of trained medical staff & microbiologist
c) Material for throat sab and culture
d) Reliable supply of penicillin
73. Primary prevention of RF
Penicillins
Penicillin V Children >27kg: 250mg b.d
<27kg: 500mg b.d or tds
oral 10days
Amoxicillin 50mg/kg dly, maximum of n1gm oral 10days
Penicillin G <27kg, 600000IU
>27kg, 1200000
IM once
Individuals with Penicillin allergy
Azithromycin 12mg/kg, max 500mg Oral 5dys
Cephalexin/Cefadroxi
l
Variable oral 10days
Clindamycin 20mg/kg/dy in 3 divided doses,
maximum if 1.8g
Oral 10days
Clarithromycin 15mg/kg/dy divide b.d Oral 10days
75. Secondary prevention
It’s the mainstay of RF and RVHD
There is an n exponential increase in predilection for ARF in
patients with ARF after episode GABHS infection
Benzathine penicillin is best antibiotic for prophylaxis
1.2million units or 600000units in < 27kg 2-4wkly
Oral penicillin V is less effective, 250mg b.d
Erythromycin 250mg b.d in penicillin allergy
77. AHA recommendation for
duration of 2o prophylaxis
Category of patients Duration
RF without carditis 5years after last attack or 21years,
whichever is longer
RF with carditis but no residual
valvular disease
10years after last attack or 21 years
whichever is longer
RF with persistent valvular disease,
evident clinically or on Echo
For 10years after last attack or
40years of age, whichever is longer .
Prophylaxis may be life long at times.
79. Management of
Complications
Major complications include
Stroke
Principle of management
1. ABCs of resuscitation
2. Optimize Cerebral Circulation in penumbra
3. Investigation: Cranial CT, ECG, Echo
4. Prevent comorbidities - infection, pneumonia, bedsores
80. Management
4. Monitor the orifices
5. Treat modifiable risk factors
6. Thrombolysis – within 3hours of Ischaemic stroke, IV rtPA 0.9mg/kg, up to
90mg maximum
7. Antiplatelets- Aspirin 300mg
Neuroprotection
8. Physiotherapy
9. Rehabilitation & Social integration
81. Management
Heart failure
Principle of management
Reduce preload
Reduce afterload
Increase cardiomyocyte contractility
Reduce salt and water retention
Treat other comorbidities
Interventional techniques eg intraortic balloon, ICD,
cardiac resynchronization.
84. Prognosis
Runs a variable course especially with valvular lesions
Reparability of valves is inconsistent
Subvalvular apparatus repair has better prognosis than
valvular lesions
The lower the degree of fibrosis of subvalvular
apparatus the btter the prognosis
Prognosis is worse with pulmonary hypertension
85. Conclusion
The impact of RVHD is felt by some but is the burden
of all. More effort obviously needs be put in to rid the
health landscape of this menace; this is economically
beneficial and aesthetically a feet at par with
international best practice.
87. References
71st WHO General AssemblyWHO provisional item, April 2018
Pathophysiology of Rheumatic Fever, Allen Burke, April 2016
Changes in Th17 associated cytokine expression in Rheumatic
heart disease. Cardiovasc Pathology. July 2015, Wen Y, Zeng z
et al
Komolafe M A, Olaogu M, Adebiyi A M, Obembe A O, Fawale
M B, Adebowale A A. Stroke risk factors among participants of
a world stroke day awareness program in South-Western
Nigeria. Niger J Clin Pract 2015;18:807-9
88. References
23rd edition, Cecil Medicine, Chapter 312, pages 2178-
2189
World heart federation guideline on treayment of
valvular heart diseases